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cxc motif chemokine ligand 6 (R&D Systems)

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R&D Systems cxc motif chemokine ligand 6
Cxc Motif Chemokine Ligand 6, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cxcl6/Recombinant+Human+CXCL6%2FGCP-2+Protein/pmc12839701-75-43-54
Average 94 stars, based on 8 article reviews

cxc motif chemokine ligand 6 - by Bioz Stars, 2026-10

94/100 stars

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Recombinant:

Article Title: The Inflammatory Microenvironment of the Aging Prostate Facilitates Cellular Proliferation and Hypertrophy
Article Snippet: .. To assess the effects of exogenous chemokines on cellular proliferation, recombinant human CXCL1 (R&D systems 275-GR), CXCL5 (R&D Systems, 254-X) or CXCL6 (R&D systems 333-GC) was added at the desired concentration in 1 ml SF HIE to each well, with parallel controls grown in SF HIE alone or complete media with serum. ..

Concentration Assay:

Sandwich ELISA:

Article Title: Ets homologous factor (EHF) has critical roles in epithelial dysfunction in airway disease
Article Snippet: .. Quantikine colorimetric sandwich ELISA for IL-8 (D800C) and CXCL6 (DGC00, both from R&D) was performed according to the manufacturer’s protocol. ..

Enzyme-linked Immunosorbent Assay:

Article Title: The Therapeutic Treatment with the GAG-Binding Chemokine Fragment CXCL9(74–103) Attenuates Neutrophilic Inflammation and Lung Dysfunction during Klebsiella pneumoniae Infection in Mice
Article Snippet: .. The cytokine IL-1β (cat. no. DY401-5) and the chemokines CXCL1 (cat. no. DY453-05), CXCL2 (cat. no. DY452-05) and CXCL6 (cat. no. MX000) were measured from the BALF supernatants by ELISA following the manufacturer’s instructions (R&D Systems, Minneapolis, MN, USA). ..

Article Title: Effect of tocilizumab on endothelial and platelet-derived CXC-chemokines and their association with inflammation and myocardial injury in STEMI patients undergoing primary PCI.
Article Snippet: Background: Tocilizumab improves myocardial salvage in ST-elevation myocardial infarction (STEMI) patients when administered before percutaneous coronary intervention (PCI).. The mechanisms underlying ischemiareperfusion injury remain unclear.. In this sub-study, we investigated whether endothelial and platelet-derived CXC chemokines are involved, as they represent inflammatory mediators from two cell types relevant to myocardial infarction.

Clinical Proteomics:

Enzyme Immunoassay:

other:

Article Title: Vascular endothelial growth factor-D improves lung vascular integrity during acute lung injury
Article Snippet: The following ligands were purchased from vendors: BMP5 (Novus Biologicals, # 615-BMC-020), VEGF-D (Cayman Chemical, #32055), Adrenomedullin (ADM)(Cayman Chemical, #24889), Angiopoietin-1 (Novus Biologicals, #923-AN), TNF-α (R&D Systems, # 10291-TA), Slit homolog 2 (SLIT2)(R&D Systems, # 8616-SL), CXCL6 (R&D Systems, # 333-GC-025/CF), Pleiotrophin (PTN)(R&D Systems, # 252-PL), and Semaphorin 6D (Sema6D)(R&D Systems, #2095-S6).

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Flow diagram of the study design. A comprehensive overview of the study workflow, illustrating the integration of bioinformatics analysis, experimental validation, and therapeutic exploration to investigate the pathogenesis of diabetic kidney disease (DKD). Gene expression datasets ( GSE30529 , GSE47184 , GSE175759 , and GSE142025 ) were analyzed to identify differentially expressed genes (DEGs) and key modules associated with DKD progression using weighted gene correlation network analysis (WGCNA). KEGG pathway enrichment analysis highlighted significant signaling pathways, and machine-learning approaches (LASSO, SVM, and RF) identified CXCL6 as the hub gene. Single-cell RNA sequencing (scRNA-seq) data further localized CXCL6 expression to proximal tubular epithelial cells in the kidney. Experimental validation was conducted using renal tissues from DKD patients and mice, as well as in vitro studies with HG-stimulated HK-2 cells and THP-1 macrophages to confirm CXCL6’s role in macrophage recruitment and inflammatory cytokine release. Virtual screening and molecular docking identified salvianolic acid B as a CXCL6-targeting inhibitor, which was shown to mitigate inflammation and macrophage migration in in vitro studies. This integrative approach bridges bioinformatics and experimental data, highlighting CXCL6’s role in DKD and its therapeutic potential.

Journal: Kidney Diseases

Article Title: CXCL6 Orchestrates Macrophage-Driven Inflammation in Diabetic Kidney Disease and Represents a Druggable Target

doi: 10.1159/000548806

Figure Lengend Snippet: Flow diagram of the study design. A comprehensive overview of the study workflow, illustrating the integration of bioinformatics analysis, experimental validation, and therapeutic exploration to investigate the pathogenesis of diabetic kidney disease (DKD). Gene expression datasets ( GSE30529 , GSE47184 , GSE175759 , and GSE142025 ) were analyzed to identify differentially expressed genes (DEGs) and key modules associated with DKD progression using weighted gene correlation network analysis (WGCNA). KEGG pathway enrichment analysis highlighted significant signaling pathways, and machine-learning approaches (LASSO, SVM, and RF) identified CXCL6 as the hub gene. Single-cell RNA sequencing (scRNA-seq) data further localized CXCL6 expression to proximal tubular epithelial cells in the kidney. Experimental validation was conducted using renal tissues from DKD patients and mice, as well as in vitro studies with HG-stimulated HK-2 cells and THP-1 macrophages to confirm CXCL6’s role in macrophage recruitment and inflammatory cytokine release. Virtual screening and molecular docking identified salvianolic acid B as a CXCL6-targeting inhibitor, which was shown to mitigate inflammation and macrophage migration in in vitro studies. This integrative approach bridges bioinformatics and experimental data, highlighting CXCL6’s role in DKD and its therapeutic potential.

Article Snippet: CXCL6 antibody (DF13470), aquaporin-1 (AQP1) antibody (sc-25287), and F4/80 antibody (70076) were purchased from Affinity Biosciences (Jiangsu, China), Santa Cruz Biotechnology (Santa Cruz, CA, USA), and Cell Signaling Technology (Boston, MA, USA), respectively.

Techniques: Biomarker Discovery, Gene Expression, Protein-Protein interactions, RNA Sequencing, Expressing, In Vitro, Migration

Screening DEGs from three datasets and using machine learning to screen hub gene. Volcano plots of DEGs from GSE30529 ( a ), GSE47184 ( b ), and GSE175759 ( c ) are presented. Venn diagrams show the intersection of DEGs across the three datasets ( d ), identifying 41 upregulated ( e ) and 5 downregulated ( f ) DEGs. g The top significant KEGG pathways in common DEGs. h The Venn diagram shows CXCL6, a hub gene that screens common DEGs using three machine-learning approaches. i The hub gene CXCL6 was significantly increased in patients with DKD compared to healthy controls (* p < 0.05).

Journal: Kidney Diseases

Article Title: CXCL6 Orchestrates Macrophage-Driven Inflammation in Diabetic Kidney Disease and Represents a Druggable Target

doi: 10.1159/000548806

Figure Lengend Snippet: Screening DEGs from three datasets and using machine learning to screen hub gene. Volcano plots of DEGs from GSE30529 ( a ), GSE47184 ( b ), and GSE175759 ( c ) are presented. Venn diagrams show the intersection of DEGs across the three datasets ( d ), identifying 41 upregulated ( e ) and 5 downregulated ( f ) DEGs. g The top significant KEGG pathways in common DEGs. h The Venn diagram shows CXCL6, a hub gene that screens common DEGs using three machine-learning approaches. i The hub gene CXCL6 was significantly increased in patients with DKD compared to healthy controls (* p < 0.05).

Techniques:

GSE142025 dataset identifies key modules associated with advanced DKD via WGCNA. a Correlation between module eigengenes and clinical traits of DKD. The turquoise module was closely related to advanced DKD. b The top 20 of significant KEGG pathways in turquoise module. c The expression level of CXCL6 in advanced DKD was significantly increased in GSE142025 database (*** p < 0.001). The mRNA expression level of CXCL6 was negatively correlated with eGFR in both the GSE30529 ( d ) and GSE175759 ( e ) databases. f Relative expression level of CXCL6 in the various cell types between healthy controls and DKD from the KIT website. g The protein expression of CXCL6 and proximal tubular epithelial marker (AQP1) in human kidney tissues of DKD and healthy control kidney using double immunofluorescence staining. h Representative CXCL6 immunohistochemical staining in healthy control kidney and renal biopsies of human DKD. Data were represented as the mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. healthy control.

Journal: Kidney Diseases

Article Title: CXCL6 Orchestrates Macrophage-Driven Inflammation in Diabetic Kidney Disease and Represents a Druggable Target

doi: 10.1159/000548806

Figure Lengend Snippet: GSE142025 dataset identifies key modules associated with advanced DKD via WGCNA. a Correlation between module eigengenes and clinical traits of DKD. The turquoise module was closely related to advanced DKD. b The top 20 of significant KEGG pathways in turquoise module. c The expression level of CXCL6 in advanced DKD was significantly increased in GSE142025 database (*** p < 0.001). The mRNA expression level of CXCL6 was negatively correlated with eGFR in both the GSE30529 ( d ) and GSE175759 ( e ) databases. f Relative expression level of CXCL6 in the various cell types between healthy controls and DKD from the KIT website. g The protein expression of CXCL6 and proximal tubular epithelial marker (AQP1) in human kidney tissues of DKD and healthy control kidney using double immunofluorescence staining. h Representative CXCL6 immunohistochemical staining in healthy control kidney and renal biopsies of human DKD. Data were represented as the mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. healthy control.

Techniques: Expressing, Marker, Control, Double Immunofluorescence Staining, Immunohistochemical staining, Staining

CXCL6 induction in DKD and screening of potential regulatory transcription factors (TFs). a CXCL6 was detected in the urine of healthy controls ( n = 12) and DKD patients ( n = 24), and the urinary CXCL6 protein concentration (µg/mg creatinine) was corrected with urinary creatinine. Linear regression shows that urinary CXCL6 levels in DKD patients are correlated with renal function (estimated glomerular filtration rate [eGFR]) ( b ), serum creatinine (Scr) ( c ), and urinary albumin-to-creatinine ratio (UACR) ( d ) compared to healthy controls. e Real-time PCR show that CXCL6 mRNA levels increased in HG-induced HK-2 cell injury. f ELISA analysis of CXCL6 in extracellular fluid of HK-2 cells revealed elevated levels following HG treatment. g Immunofluorescence staining of CXCL6 (red) in HK-2 cells with or without HG-treated. h t-SNE visualization of regulon activity in PCT cells, comparing diabetic kidney disease (DKD) and control (CTRL) groups. i Heatmap analysis delineated differential activation patterns of TFs and regulons in DKD compared to CTRL. j Area under the curve scores of the FOXP2 (18 g) target gene set show elevated activity in DKD, suggesting enhanced transcriptional regulation (upper). t-SNE visualization of binary regulon activity reveals distinct clustering, confirming disease-specific FOXP2 activation in DKD compared to CTRL (bottom). k A schematic illustration depicts the FOXP2 motif within the promoter region of the CXCL6 locus. Data were represented as the mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. healthy control or NC. PCT, proximal tubule cell.

Journal: Kidney Diseases

Article Title: CXCL6 Orchestrates Macrophage-Driven Inflammation in Diabetic Kidney Disease and Represents a Druggable Target

doi: 10.1159/000548806

Figure Lengend Snippet: CXCL6 induction in DKD and screening of potential regulatory transcription factors (TFs). a CXCL6 was detected in the urine of healthy controls ( n = 12) and DKD patients ( n = 24), and the urinary CXCL6 protein concentration (µg/mg creatinine) was corrected with urinary creatinine. Linear regression shows that urinary CXCL6 levels in DKD patients are correlated with renal function (estimated glomerular filtration rate [eGFR]) ( b ), serum creatinine (Scr) ( c ), and urinary albumin-to-creatinine ratio (UACR) ( d ) compared to healthy controls. e Real-time PCR show that CXCL6 mRNA levels increased in HG-induced HK-2 cell injury. f ELISA analysis of CXCL6 in extracellular fluid of HK-2 cells revealed elevated levels following HG treatment. g Immunofluorescence staining of CXCL6 (red) in HK-2 cells with or without HG-treated. h t-SNE visualization of regulon activity in PCT cells, comparing diabetic kidney disease (DKD) and control (CTRL) groups. i Heatmap analysis delineated differential activation patterns of TFs and regulons in DKD compared to CTRL. j Area under the curve scores of the FOXP2 (18 g) target gene set show elevated activity in DKD, suggesting enhanced transcriptional regulation (upper). t-SNE visualization of binary regulon activity reveals distinct clustering, confirming disease-specific FOXP2 activation in DKD compared to CTRL (bottom). k A schematic illustration depicts the FOXP2 motif within the promoter region of the CXCL6 locus. Data were represented as the mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. healthy control or NC. PCT, proximal tubule cell.

Techniques: Protein Concentration, Filtration, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Staining, Activity Assay, Control, Activation Assay

Levels of CXCL6 were increased in db/db mice. a Analysis of blood glucose levels. b Analysis of serum creatinine (Scr) levels. c Analysis of urinary albumin-to-creatinine ratio (UACR). d CXCL6 was detected in the urine of db/m and db/db mice ( n = 6), with the urinary CXCL6 protein concentration corrected by urinary creatinine (µg/mg creatinine). e , f Linear regression analysis reveals a correlation between urinary CXCL6 and Scr and UACR in db/db mice. g Histological observations of kidney sections stained with PAS. IHC and quantification of CXCL6 ( h ) and F4/80 ( i ) in db/db renal tissue. The levels of mRNA for CXCL6, a-SMA, and FN were analyzed by real-time PCR ( j ), and linear regression analysis showed that the mRNA level of CXCL6 is also correlated with a-SMA ( k ) and FN ( l ) in db/db mice. Data represent the mean ± SEM of 6 mice in vivo. Statistically significant differences were determined by independent sample t test and one-way analysis of variance (ANOVA) followed by Tukey’s post hoc test. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. db/m.

Journal: Kidney Diseases

Article Title: CXCL6 Orchestrates Macrophage-Driven Inflammation in Diabetic Kidney Disease and Represents a Druggable Target

doi: 10.1159/000548806

Figure Lengend Snippet: Levels of CXCL6 were increased in db/db mice. a Analysis of blood glucose levels. b Analysis of serum creatinine (Scr) levels. c Analysis of urinary albumin-to-creatinine ratio (UACR). d CXCL6 was detected in the urine of db/m and db/db mice ( n = 6), with the urinary CXCL6 protein concentration corrected by urinary creatinine (µg/mg creatinine). e , f Linear regression analysis reveals a correlation between urinary CXCL6 and Scr and UACR in db/db mice. g Histological observations of kidney sections stained with PAS. IHC and quantification of CXCL6 ( h ) and F4/80 ( i ) in db/db renal tissue. The levels of mRNA for CXCL6, a-SMA, and FN were analyzed by real-time PCR ( j ), and linear regression analysis showed that the mRNA level of CXCL6 is also correlated with a-SMA ( k ) and FN ( l ) in db/db mice. Data represent the mean ± SEM of 6 mice in vivo. Statistically significant differences were determined by independent sample t test and one-way analysis of variance (ANOVA) followed by Tukey’s post hoc test. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. db/m.

Techniques: Protein Concentration, Staining, Real-time Polymerase Chain Reaction, In Vivo

CXCL6 was chemotactic to macrophages and increased the release of inflammatory cytokines in macrophages. a Uniform manifold approximation and projection (UMAP) plot showing cell cluster identities and the cell cluster abundance in control and DKD. ENDO, endothelial cells; MES, mesangial cells; PODO, podocytes; CFH+, complement factor H-positive cells; LOH, loop of Henle; CD, collecting duct; PC, principal cell; IC, intercalated cell; DCT, distal convoluted tubule; PCT, proximal tubular cells; LEUK, leukocyte. b t-SNE plot showing CXCR2 in macrophages. c The protein levels of CXCR2 in THP-1 cells were significantly upregulated following stimulation with CXCL6. d Flow cytometry analysis showed that CXCL6 cytokines could polarize THP-1 cells into pro-inflammatory macrophages. e The protein expression of CXCR2 and pro-inflammatory macrophage marker (iNOS) in human kidney tissues of DKD and healthy control kidney using double immunofluorescence staining. f The mRNA expression levels of TNF-a, IL-6, and IL-23 in THP-1 cells after CXCL6 stimulation were detected by real-time PCR. g Transwell migration assays showed that the addition of CXCL6 cytokines to extracellular fluid increased the migration of THP-1 cells. Data represent the mean ± SEM. of at least three independent experiments in vitro. Statistically significant differences were determined by independent sample t test and one-way analysis of variance (ANOVA) followed by Tukey’s post hoc test. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. MΦ.

Journal: Kidney Diseases

Article Title: CXCL6 Orchestrates Macrophage-Driven Inflammation in Diabetic Kidney Disease and Represents a Druggable Target

doi: 10.1159/000548806

Figure Lengend Snippet: CXCL6 was chemotactic to macrophages and increased the release of inflammatory cytokines in macrophages. a Uniform manifold approximation and projection (UMAP) plot showing cell cluster identities and the cell cluster abundance in control and DKD. ENDO, endothelial cells; MES, mesangial cells; PODO, podocytes; CFH+, complement factor H-positive cells; LOH, loop of Henle; CD, collecting duct; PC, principal cell; IC, intercalated cell; DCT, distal convoluted tubule; PCT, proximal tubular cells; LEUK, leukocyte. b t-SNE plot showing CXCR2 in macrophages. c The protein levels of CXCR2 in THP-1 cells were significantly upregulated following stimulation with CXCL6. d Flow cytometry analysis showed that CXCL6 cytokines could polarize THP-1 cells into pro-inflammatory macrophages. e The protein expression of CXCR2 and pro-inflammatory macrophage marker (iNOS) in human kidney tissues of DKD and healthy control kidney using double immunofluorescence staining. f The mRNA expression levels of TNF-a, IL-6, and IL-23 in THP-1 cells after CXCL6 stimulation were detected by real-time PCR. g Transwell migration assays showed that the addition of CXCL6 cytokines to extracellular fluid increased the migration of THP-1 cells. Data represent the mean ± SEM. of at least three independent experiments in vitro. Statistically significant differences were determined by independent sample t test and one-way analysis of variance (ANOVA) followed by Tukey’s post hoc test. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. MΦ.

Techniques: Control, Flow Cytometry, Expressing, Marker, Double Immunofluorescence Staining, Real-time Polymerase Chain Reaction, Migration, In Vitro

The potential pathways by which CXCL6 regulates the polarization and migration of THP-1 cells. a Volcano plot of differential gene expression between MΦ and MΦ+CXCL6 THP-1 cells. b Results of KEGG pathway enrichment analysis based on RNA-seq of THP-1 cells. c GSEA results based on the RNA-Seq data. d Representative Western blot of CXCR2 protein expression in coculture models in vitro. e The mRNA expressions of TNF-a, IL-6, and IL-23 in THP-1 cells were analyzed by RT-qPCR in HG-induced HK-2 cells with or without Si-CXCL6. f The migration of THP-1 cells in HG-induced HK-2 cells with or without Si-CXCL6 was analyzed by Transwell migration assay. g Schematic diagram of the virtual screening-based strategy for exploring anti-renal inflammatory TCM monomers targeting CXCL6. h Molecular docking of salvianolic acid B to the catalytic core of CXCL6. Data represent the mean ± SEM. of at least three independent experiments in vitro. Statistically significant differences were determined by independent sample t test and one-way analysis of variance (ANOVA) followed by Tukey’s post hoc test. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. NC. # p < 0.05, ## p < 0.01, ### p < 0.001 vs. HG. NC, normal control; HG, high glucose.

Journal: Kidney Diseases

Article Title: CXCL6 Orchestrates Macrophage-Driven Inflammation in Diabetic Kidney Disease and Represents a Druggable Target

doi: 10.1159/000548806

Figure Lengend Snippet: The potential pathways by which CXCL6 regulates the polarization and migration of THP-1 cells. a Volcano plot of differential gene expression between MΦ and MΦ+CXCL6 THP-1 cells. b Results of KEGG pathway enrichment analysis based on RNA-seq of THP-1 cells. c GSEA results based on the RNA-Seq data. d Representative Western blot of CXCR2 protein expression in coculture models in vitro. e The mRNA expressions of TNF-a, IL-6, and IL-23 in THP-1 cells were analyzed by RT-qPCR in HG-induced HK-2 cells with or without Si-CXCL6. f The migration of THP-1 cells in HG-induced HK-2 cells with or without Si-CXCL6 was analyzed by Transwell migration assay. g Schematic diagram of the virtual screening-based strategy for exploring anti-renal inflammatory TCM monomers targeting CXCL6. h Molecular docking of salvianolic acid B to the catalytic core of CXCL6. Data represent the mean ± SEM. of at least three independent experiments in vitro. Statistically significant differences were determined by independent sample t test and one-way analysis of variance (ANOVA) followed by Tukey’s post hoc test. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. NC. # p < 0.05, ## p < 0.01, ### p < 0.001 vs. HG. NC, normal control; HG, high glucose.

Techniques: Migration, Gene Expression, RNA Sequencing, Western Blot, Expressing, In Vitro, Quantitative RT-PCR, Transwell Migration Assay, Control

In vitro experiments showed that inhibition of CXCL6 secretion by Sal-B can alleviate the release of inflammatory cytokines in macrophages and the chemotaxis of macrophages. a CCK-8 measured drug toxicity and optimal concentration of salvianolic acid B. b Representative immunofluorescence staining showed that salvianolic acid B treatment reduced the CXCL6 abundance in HG-treated HK-2 cells ( n = 3). Scale bar = 20 μm. c Schematic diagram of coculture of HK-2 cells and THP-1 cells. d Representative Western blot and quantification of CXCR2 protein expression in coculture models in vitro. e The mRNA expressions of TNF-a, IL-6, and IL-23 in THP-1 cells were analyzed by RT-qPCR in HG-induced HK-2 cells with or without Sal-B. f The migration of THP-1 cells in HG-induced HK-2 cells with or without Sal-B was analyzed by Transwell migration assay. Data represent the mean ± SEM. of at least three independent experiments in vitro. Statistically significant differences were determined by independent sample t test and one-way analysis of variance (ANOVA) followed by Tukey’s post hoc test. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. NC and Sal-B. p < 0.05, p < 0.01, p < 0.001, vs. HG. NC, normal control; HG, high glucose; Sal-B, salvianolic acid B.

Journal: Kidney Diseases

Article Title: CXCL6 Orchestrates Macrophage-Driven Inflammation in Diabetic Kidney Disease and Represents a Druggable Target

doi: 10.1159/000548806

Figure Lengend Snippet: In vitro experiments showed that inhibition of CXCL6 secretion by Sal-B can alleviate the release of inflammatory cytokines in macrophages and the chemotaxis of macrophages. a CCK-8 measured drug toxicity and optimal concentration of salvianolic acid B. b Representative immunofluorescence staining showed that salvianolic acid B treatment reduced the CXCL6 abundance in HG-treated HK-2 cells ( n = 3). Scale bar = 20 μm. c Schematic diagram of coculture of HK-2 cells and THP-1 cells. d Representative Western blot and quantification of CXCR2 protein expression in coculture models in vitro. e The mRNA expressions of TNF-a, IL-6, and IL-23 in THP-1 cells were analyzed by RT-qPCR in HG-induced HK-2 cells with or without Sal-B. f The migration of THP-1 cells in HG-induced HK-2 cells with or without Sal-B was analyzed by Transwell migration assay. Data represent the mean ± SEM. of at least three independent experiments in vitro. Statistically significant differences were determined by independent sample t test and one-way analysis of variance (ANOVA) followed by Tukey’s post hoc test. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. NC and Sal-B. p < 0.05, p < 0.01, p < 0.001, vs. HG. NC, normal control; HG, high glucose; Sal-B, salvianolic acid B.

Techniques: In Vitro, Inhibition, Chemotaxis Assay, CCK-8 Assay, Concentration Assay, Immunofluorescence, Staining, Western Blot, Expressing, Quantitative RT-PCR, Migration, Transwell Migration Assay, Control

Interferon (IFN)-activated fibroblasts (FBs) are enriched in SS skin. A, Number of significantly upregulated genes (adjusted P value [ P adj ] < .05) in patients with SS versus patients with HC for each cell type. Differential expression analysis was performed using DESeq2. Pseudobulked data were used to control for cell number. B, Dimensionality reduction and unsupervised clustering of FBs, colored by subset. C, Expression of the top 4 marker genes per FB subset. D, Proportion of FB subsets for each condition. E, Pathway analysis inferring upstream transcription factors regulating gene expression for each cluster. F, Scaled expression of neutrophil chemokine CXCR2 ligands ( CXCL1, CXCL2, CXCL3, CXCL5, CXCL6 , and CXCL8 ) and CXCR4 ligand ( CXCL12 ) across cell types for each condition. Keratinocytes, eccrine cells, and melanocytes were combined into the category epithelial. DCs, pDCs, mast cells, and myeloid cells were combined into the category myeloid. Plasma cells and lymphoid cells were combined into the category lymphoid. Vascular endothelial cells, lymphatic endothelial cells, and mural cells were combined into the category endothelial-mural. Proliferating cells and adipocytes were excluded. Error bars represent SEMs.

Journal: The Journal of allergy and clinical immunology

Article Title: Positionally distinct interferon-stimulated dermal immune-acting fibroblasts promote neutrophil recruitment in Sweet syndrome

doi: 10.1016/j.jaci.2025.05.029

Figure Lengend Snippet: Interferon (IFN)-activated fibroblasts (FBs) are enriched in SS skin. A, Number of significantly upregulated genes (adjusted P value [ P adj ] < .05) in patients with SS versus patients with HC for each cell type. Differential expression analysis was performed using DESeq2. Pseudobulked data were used to control for cell number. B, Dimensionality reduction and unsupervised clustering of FBs, colored by subset. C, Expression of the top 4 marker genes per FB subset. D, Proportion of FB subsets for each condition. E, Pathway analysis inferring upstream transcription factors regulating gene expression for each cluster. F, Scaled expression of neutrophil chemokine CXCR2 ligands ( CXCL1, CXCL2, CXCL3, CXCL5, CXCL6 , and CXCL8 ) and CXCR4 ligand ( CXCL12 ) across cell types for each condition. Keratinocytes, eccrine cells, and melanocytes were combined into the category epithelial. DCs, pDCs, mast cells, and myeloid cells were combined into the category myeloid. Plasma cells and lymphoid cells were combined into the category lymphoid. Vascular endothelial cells, lymphatic endothelial cells, and mural cells were combined into the category endothelial-mural. Proliferating cells and adipocytes were excluded. Error bars represent SEMs.

Article Snippet: The TaqMan primers included RPLP0 (Thermo Fisher Scientific; catalog no. Hs004200895_gh), CXCL1 (Thermo Fisher Scientific; catalog no. Hs00236937_m1), CXCL2 (Thermo Fisher Scientific; catalog no. Hs00234140_m1), CXCL3 (Thermo Fisher Scientific; catalog no. Hs00171061_m1), CXCL5 (Thermo Fisher Scientific; catalog no. Hs00982282_m1), CXCL6 (Thermo Fisher Scientific; catalog no. Hs00237017_m1), and CXCL8 (Thermo Fisher Scientific; catalog no. Hs00174103_m1).

Techniques: Quantitative Proteomics, Control, Expressing, Marker, Gene Expression, Clinical Proteomics

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cxc motif chemokine ligand 6 (R&D Systems)

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